Fexofenadine is the therapeutically active compound of the originally marketed drug, terfenadine, which upon accumulation was found to be associated with prolonged QTc intervals, torsades de point, and sudden death (1,2,3,4). Less than 5% of the drug, fexofenadine, is metabolized, therefore, the cytochrome P4503A interactions are not a factor. However, concomitant administration of fexofenadine with the potent CYP3A inhibitors (also p-glycoprotein inhibitors), erythromycin and ketoconazole, leads to a substantial increase in fexofenadine AUC. The precise mechanism of this interaction is not clear, but may involve the inhibition of p-glycoprotein. The primary goal of this study is to determine if rifampin alters the clearance of fexofenadine and if so, whether age has any effect on the clearance. Changes in fexofenadine clearance may reflect alteration in p-glycoprotein activity.